The correlation of hepatitis B virus pre-S mutation with cellular oxidative DNA damage in hepatocellular carcinoma
- Authors
- Gwak, G.-Y.[Gwak, G.-Y.]; Lee, D.H.[ Lee, D.H.]; Moon, T.G.[ Moon, T.G.]; Choi, M.S.[Choi, M.S.]; Lee, J.H.[Lee, J.H.]; Koh, K.C.[Koh, K.C.]; Paik, S.W.[Paik, S.W.]; Park, C.K.[Park, C.K.]; Joh, J.-W.[Joh, J.-W.]; Yoo, B.C.[Yoo, B.C.]
- Issue Date
- 2008
- Keywords
- 8-OxoG; ER stress; Hepatitis B virus; Hepatocellular carcinoma; OGG1; Pre-S mutation
- Citation
- Hepato-Gastroenterology, v.55, no.88, pp.2028 - 2032
- Indexed
- SCOPUS
- Journal Title
- Hepato-Gastroenterology
- Volume
- 55
- Number
- 88
- Start Page
- 2028
- End Page
- 2032
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/83176
- ISSN
- 0172-6390
- Abstract
- Background/Aims: Recent research has proposed a role for HBV pre-S mutation in the development of HCC. Although the mechanism is not clear, pre-S mutant-induced endoplasmic reticulum (ER) stress and oxidative DNA damage may participate in this process. Therefore, we investigated the correlation of HBV pre-S mutation with ER stress and cellular oxidative DNA damage in HBV-related HCC patients. Methodology: Thirty HBV-related HCC patients and 8 control patients were included. HBV DNA was extracted from sera and the HBV S coding region was analyzed by PCR and sequencing. Immunohistochemical staining for 8-oxoG and OGG1 were performed in HCC and non-neoplastic tissues. Results: Study subjects were categorized into three groups: the pre-S mutant HBV-infected HCC patients (group 1, n=20), wild-type HBV-infected HCC patients (group 2, n=10) and HBV non-infected patients (group 3, n=8). The expression level of 8-oxoG and OGG1 in non-neoplastic tissue was higher in group 1/2 than in group 3; however, there was no significant difference between group 1 and 2. There was no significant difference in 8-oxoG/OGG1 expressions between HCC and non-neoplastic tissues. Conclusions: The present study did not support a pathophysiologic role for HBV pre-S mutation, related to ER stress and oxidative DNA damage, in hepatocarcinogenesis. © H.G.E. Update Medical Publishing S.A., Athens-Stuttgart.
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